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Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice
RESEARCH | Updated：2025-12-13
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    • Elevated FBXL6 activates both wild-type KRAS and mutant KRASG12D and drives HCC tumorigenesis via the ERK/mTOR/PRELID2/ROS axis in mice

    • “In the field of liver cancer research, this study investigates how FBXL6 regulates KRAS and KRASG12D activity in hepatocellular carcinoma. Expert established the FBXL6/KRAS/ERK/mTOR/PRELID2/ROS axis, which provides a potential therapeutic strategy to treat aggressive liver cancer.”
    • Hao-Jun Xiong , Hong-Qiang Yu , Jie Zhang , Lei Fang , Di Wu , Xiao-Tong Lin , Chuan-Ming Xie
    • Military Medical Research Vol. 11, Issue 6, Pages: 818-838(2024)

    • DOI： 10.1186/s40779-023-00501-8     

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